Long Covid in Vaccinated vs. Unvaccinated Populations 

For most people, mild or moderate COVID-19 lasts for about two weeks. In others, however, health problems linger even after they are no longer testing positive for the illness; the long-term effects of coronavirus can persist for months or even years (Johns Hopkins Medicine, 2022). The World Health Organization describes post-COVID-19 condition, known colloquially as “long COVID,” as symptoms that persist or return “3 months from the onset of COVID-19… last for at least 2 months and cannot be explained by an alternative diagnosis” (WHO, 2021). Such symptoms can include fatigue, cognitive dysfunction (problems with thinking and memory), and shortness of breath, among others (WHO, 2021). They may be new following initial recovery from an acute COVID-19 episode, or they may persist from the initial illness; symptoms can also fluctuate or relapse over time. While getting vaccinated for COVID-19 does lower the risk of COVID infection, research concerning long COVID in vaccinated versus unvaccinated populations is ongoing. 

A recent study published in JAMA found that “among health care workers with SARS-CoV-2 infections not requiring hospitalization, 2 or 3 doses of vaccine, compared with no vaccination, were associated with lower long COVID prevalence” (Azzolini et al., 2022). Researchers from the Humanitas Research Hospital in Milan, Italy, conducted an observational cohort study from March 2020 to April 2022 among individuals working in 9 Italian health care facilities. All health care workers underwent weekly (in COVID wards) or biweekly (in other wards) PCR tests for COVID infection and had received three doses of the Pfizer-BioNTech vaccine over the course of 2021 (Azzolini et al., 2022). Researchers defined long COVID as reporting “at least 1 SARS-CoV-2-related symptom with a duration of more than 4 weeks” (Azzolini et al., 2022). Out of 2,560 participants, 29% had COVID-19, of which 31% had long COVID. Researchers categorized participants who caught COVID-19 by whether they were vaccinated at the time of infection and then calculated rates of long COVID for each group. Notably, having received more vaccine doses was associated with lower prevalence of long COVID: 41.8% when unvaccinated, 30.0% when having received 1 dose, 17.4% with 2 doses, and 16.0% with 3 doses of the vaccine (Azzolini et al., 2022). 

Long COVID has proved quite difficult to study, in part because the array of symptoms makes it hard to define. Even determining how common it is has been challenging: while some studies have previously suggested that long COVID occurs in as many as 30% of individuals infected with the virus, other results show much lower prevalence (Yoo et al., 2022; Stephenson et al., 2021). For example, a November 2021 study of around 4.5 million people treated at US Department of Veterans Affairs Hospitals suggests that the number is “7% overall and lower than that for those who were not hospitalized” (Xie et al., 2021). To date, there have been more than 93 million COVID-19 infections in the US alone (NYT, 2022). If even a small percentage of those infections turn into long COVID, “that’s a staggeringly high number of people affected by a disease that remains mysterious” (Reardon, 2022). To that end, some researchers suggest that vaccination alone might not be the best way to reduce the risk of long-term effects of Covid. Since research on long COVID is evolving, other COVID mitigation strategies remain important to the health of individuals worldwide. 


Al-Aly, Z., Bowe, B., & Xie, Y. (2022). Long COVID after breakthrough SARS-CoV-2 infection. Nature Medicine, 28(7), 1461–1467. 

Azzolini, E., Levi, R., Sarti, R., Pozzi, C., Mollura, M., Mantovani, A., & Rescigno, M. (2022). Association Between BNT162b2 Vaccination and Long COVID After Infections Not Requiring Hospitalization in Health Care Workers. JAMA, 328(7), 676–678. 

Long COVID: Long-Term Effects of COVID-19. (2022, June 14). Johns Hopkins Medicine. 

Reardon, S. (2022). Long COVID risk falls only slightly after vaccination, huge study shows. Nature. 

Stephenson, T., Shafran, R., & Rojas, N. (2021, August 10). Long COVID – the physical and mental health of children and non-hospitalised young people 3 months after SARS-CoV-2 infection; a national matched cohort study (The CLoCk) Study. Research Square. 

Times, T. N. Y. (2020, March 3). Coronavirus in the U.S.: Latest Map and Case Count. The New York Times. 

WHO: Clinical Services and Systems, Communicable Diseases, Technical Advisory Group on SARS-CoV-2 Virus Evolution. (2021, October 6). A clinical case definition of post COVID-19 condition by a Delphi consensus. World Health Organization. 

Xie, Y., Bowe, B., & Al-Aly, Z. (2021). Burdens of post-acute sequelae of COVID-19 by severity of acute infection, demographics and health status. Nature Communications, 12(1), 6571. 

Yoo, S. M., Liu, T. C., Motwani, Y., Sim, M. S., Viswanathan, N., Samras, N., Hsu, F., & Wenger, N. S. (2022). Factors Associated with Post-Acute Sequelae of SARS-CoV-2 (PASC) After Diagnosis of Symptomatic COVID-19 in the Inpatient and Outpatient Setting in a Diverse Cohort. Journal of General Internal Medicine, 37(8), 1988–1995. 


Post Dural Puncture Headache 

Neuraxial anesthesia refers to the administration of local anesthetic in or around the central nervous system (CNS), which blocks sensation for a certain region of the body. This type of anesthesia is often used for procedures in the lower body, sometimes in combination with general anesthesia (1). One potential side effect of neuraxial anesthesia and some spinal procedures is post dural puncture headache, and though advancements in knowledge and technology have drastically reduced its incidence, this condition causes serious discomfort and can negatively impact patient recovery (1-4). 

To understand post dural puncture headache, it is necessary to understand the anatomy of the meninges in the spine. Within the spinal column, the spinal cord is covered by three membranes – “meninges” – which are the dura mater (outermost), arachnoid mater, and pia mater (innermost). Cerebrospinal fluid (CSF) circulates within the meninges, as well as certain parts of the brain (1-3). Epidural anesthesia, which is one of the major subcategories of neuraxial anesthesia, delivers anesthetic to the space outside of the dura mater. Spinal anesthesia, the other major subcategory, delivers anesthetic to the space between the arachnoid and pia mater (1,2). 

Procedures that puncture the meninges, such as the administration of spinal anesthesia, have been linked to severe headaches when the patient is in the upright position. Procedures in the epidural space may inadvertently puncture the dura and cause post dural puncture headache as well (1-5). Patients may also experience dizziness, nausea and vomiting, and auditory or visual disturbances (2,3,5). There are several related hypotheses as to what causes these symptoms. Meningeal puncture allows CSF to leak out faster than it can be replenished naturally. Headache may be caused by resulting intracranial hypotension, compensatory vasodilation of vessels in the CNS, and/or mechanical stimulation of pain-sensitive structures in the skull due to the changing environment (2-5). Regarding the fact that post dural puncture headache tends to be more severe when upright, this is thought to be because the decreased level of CSF is magnified by gravity pulling the remaining fluid down and away from the brain. 

Several risk factors for post dural puncture headache have been identified. Young adults, women, lower BMI individuals, and those who experience chronic headache are more likely to experience this side effect after a spinal procedure. A more experienced provider performing the procedure, proper technique as elucidated by research, and smaller needle size are associated with lower risk (2,3,5). Accurate needle positioning can be more challenging in patients with obesity due difficulty palpating bony landmarks, which can lead to accidental dural puncture, but otherwise, higher BMI is actually associated with lower risk – one hypothesis for this pattern is that higher BMI results in higher intra-abdominal pressure that helps to counteract CSF leakage (3). 

The incidence of post dural puncture headache at the advent of neuraxial anesthesia was extremely high. However, research has revealed ways in which spinal procedure techniques can be modified to improve outcomes. These include smaller needles, non-cutting needles, and provider skill in the form of first pass success (3,5). 

Treatment for this condition is still a topic of research; currently accepted approaches include inducing vasoconstriction (such as with caffeine) and placing a “blood patch” to generate a clot that blocks the puncture. Note, however, that post dural puncture headache does resolve on its own given time (2,4). 


  1. Olawin AM, Das JM. Spinal Anesthesia. StatPearls [Internet]. 2021. 
  1. Turnbull DK, Shepherd DB. Post‐dural puncture headache: pathogenesis, prevention and treatment. British Journal of Anaesthesia. 2003; 91(5):718–729. DOI:10.1093/bja/aeg231 
  1. Harrington BE, Reina MA. “Postdural puncture headache.” NYSORA. (n.d.). 
  1. Committee on Obstetric Anesthesia. “Statement on Post-Dural Puncture Headache Management.” ASA. 2021. 
  1. Kim JE, Kim SH, Han RJW, et al. Postdural Puncture Headache Related to Procedure: Incidence and Risk Factors After Neuraxial Anesthesia and Spinal Procedures. Pain Medicine. 2021;22(6):1420-1425. DOI:10.1093/pm/pnaa437 

Health System Responses to Data Breaches 

One of the fundamental beliefs within the American medical system is that patients have the right to privacy. This right is increasingly challenged by cyberattacks, and thus how the health system should respond to data breaches is a key area of work. According to the North American Association for Central Cancer Registries,  

“Confidentiality is the cancer registry’s responsibility to the patients whose data are in the database and is of paramount concern to all cancer registries. There may be no greater threat to the operation and maintenance of a cancer registry than an actual or perceived breach of confidentiality. In fact, an actual or perceived breach of confidentiality in one registry may threaten all registries.”1 

That is to say – to threaten this privacy is to threaten the practice of keeping patient records at all, which in turn threatens the practice of medicine as we know it. 

Although there are many measures of security to protect both the healthcare workplace and its respective databases, data breaches are an unfortunate eventuality. A data breach can occur for any number of reasons: an accidental violation of HIPAA protocol, for example, or a pre-planned attack by a hacker hoping to negotiate ransom. No matter the type of breach, it is critical that healthcare providers have both protection against breaches as well as a response protocol. 

According to the CDC, successful management of a data breach starts long before the incident even occurs. In other words, a pre-written detailed plan in the case of a data breach should be organized and shared amongst healthcare employees to ensure rapid response. Once such a plan has been drafted, agreed upon, and taught, “it is the program’s responsibility to execute its response plan.”2 Failure to do so increases the risk of violating legislative protocol,3 worsening the impact of the original breach, and enabling subsequent breaches. These in turn can cause the healthcare institution to lose credibility with patients and other healthcare providers, as well as cause harm to patients themselves 

One key part of said plan is a breach response team (BRT), or a group of people with the designated responsibility of investigating suspected data breaches in a health system. It is advisable that the members of such team have a background in computer science or information technology, which will allow them to troubleshoot each incident.2 Familiarity with each facility’s technology and security measures is also a prerequisite for being a member of the BRT. Duties of the BRT can include (but is not limited to) developing detection programs and methods for reporting breaches, responding to and tracking suspected breaches, evaluating response tactics, and notifying individuals whose privacy may have been affected by the data breach. However, it is not the job of the BRT alone to manage data breaches. The workplace as a whole must be well-educated and ready to respond in the case of a breach. If proper education is giving and non-compliance leads to a data breach, then that individual employee is responsible and can face both legal and corporate charges. Even an accidental breach may culminate in loss of employment and the potential for legal repercussions. 

Clearly, protection of private data is integral to the function and purpose of a healthcare facility. Therefore, responding to data breaches in a timely, effective, and appropriate manner is of utmost importance. 


1 Standards for completeness, quality, analysis, and management of data, Volume III. NAACCR. (2019, September 12). Retrieved from  

2 Centers for Disease Control and Prevention. (2021, January 20). Data breach response. Centers for Disease Control and Prevention. Retrieved from  

3 (OCR), O. for C. R. (2021, June 28). Breach notification rule. Retrieved from 


R-Ketamine vs. S-Ketamine

(R,S)-ketamine is a N-methyl-ᴅ-aspartate (NMDA) receptor antagonist and a commonly used anesthetic agent worldwide. In the late 1990s, studies and case reports began highlighting this drug’s rapid-acting and sustained antidepressant effects, a major discovery in the research of mood disorders [1]. (R,S)-ketamine is a mixture of the two enantiomers R- and S-ketamine, which predominantly differ in their binding properties [2]. S-ketamine has an approximately fourfold greater affinity for the phencyclidine site of the NMDA receptor than R-ketamine as well as strong anti-depressant effects but also strong psychomimetic side effects such as confusion, euphoria, perceptual difficulties, or mood elevation. On the other hand, R-ketamine is generally associated with a milder but longer-lasting antidepressant effect [2,3].

In 2017, a PET study on conscious monkeys found a reduction of dopamine D2/3 binding potential in the striatum following S-ketamine administration, but not R-ketamine [4]. In 2000, a research team in Japan used monkey brains and found [11C] raclopride could be used in PET to detect release of endogenous dopamine from presynaptic terminals [5]. Applying this finding, researchers at the Central Research Laboratory in Japan (2017) found marked radioactivity in the striatum of S-ketamine-treated animals, suggesting S-ketamine causes significant release of dopamine but prevents it from binding to its receptors [4]. The excessive dopamine may also be the cause of the psychosis and dissociation associated with chronic S-ketamine administration. In healthy subjects, an infusion of S-ketamine produced a dissociative state, changes in mood and sensory perception, difficulty in reality appraisal, and ego inflation [6]. Despite an increasing number of studies arguing in favor of ketamine’s role in treating depressive disorders, the drug’s abuse potential is its greatest limitation. The conditioned place preference test (CPP) is a widely used behavioral model designed to assess a drug’s rewarding, aversive, or addicting effects [7].  A 2015 preclinical study found ketamine (the racemic combination) increased scores on the CPP test, suggesting ketamine itself is rewarding [8]. Another preclinical study used the same assessment and found similar increases after S-ketamine administration, but not R-ketamine, indicating potential abuse liability of S-ketamine in particular [9].

Parvalbumin (PV) positive cells are GABAergic interneurons that rely on Ca2+ binding for proper functioning [10]. A reduction in PV-neurotransmission is associated with neuropsychiatric disorders such as Alzheimer’s Disease, autism spectrum disorder, schizophrenia, and substance use disorder. In 2016, a research team in Japan used PV-immunohistochemistry to assess the effect of intermittent ketamine administration. They observed a significant decrease in PV-immunoreactivity in the prelimbic and infralimbic areas of the prefrontal cortex, as well as the CA1, CA3, and dentate gyrus of the hippocampus after intermittent administrations of S-ketamine, but not R-ketamine [11]. These results correlate with earlier findings using the same methods but with single-dose administrations of the respective drugs [8].  These studies suggest S-ketamine plays a role in the loss of PV-positive cells, which is associated with psychiatric presentations [11].

S-ketamine is metabolized to its major metabolite, S-norketamine, by cytochrome P450 enzymes. Like S-ketamine, S-norketamine induces strong antidepressant effects in murine models of depression. S-norketamine significantly attenuated the reduced dendritic spine density in the prelimbic area, the CA3, and the dentate gyrus in mice exposed to chronic social defeat stress. In the same regions, S-norketamine also improved reduced levels of BDNF protein, a marker of neuroplasticity [12]. Unlike S-ketamine, its metabolite does not show psychomimetic effects such as increased locomotion, hyperactivity, or increased scores on the conditioned place preference test. S-norketamine also had no effect on the proportion of PV-positive cells in the prefrontal cortex [9,12]. These results suggest that S-norketamine may be a more promising therapeutic approach, if it can be successfully stabilized and administered.

Although the US and Europe approved an S-ketamine based nasal spray for treatment-resistant depression, several concerns have been raised, including its safety for pediatric patients and its numerous side effects [13,14]. A recent pilot study demonstrated R-ketamine produced sustained antidepressant effects without side effects such as dissociation [9,15]. With ketamine’s different enantiomers and metabolites, more research on their effects and applications is warranted. 


  1. Abdallah, C. G., Sanacora, G., Duman, R. S., & Krystal, J. H. (2018). The Neurobiology of Depression, Ketamine and Rapid-acting Antidepressants: Is it Glutamate Inhibition or Activation? Pharmacology & Therapeutics190, 148–158.
  2. Paul, R., Schaaff, N., Padberg, F., Möller, H.-J., & Frodl, T. (2009). Comparison of Racemic Ketamine and S-ketamine in Treatment-resistant Major Depression: Report of Two Cases. The World Journal of Biological Psychiatry: The Official Journal of the World Federation of Societies of Biological Psychiatry10(3), 241–244.
  3. Zhang, J., Li, S., & Hashimoto, K. (2014). R(−)Ketamine shows Greater Potency and Longer Lasting Antidepressant Effects than S (+)Ketamine. Pharmacology Biochemistry and Behavior116, 137–141.
  4. Hashimoto, K., Kakiuchi, T., Ohba, H., Nishiyama, S., & Tsukada, H. (2017). Reduction of Dopamine D2/3 Receptor Binding in the Striatum after a Single Administration of Esketamine, but not R-Ketamine: A PET study in Conscious Monkeys. European Archives of Psychiatry and Clinical Neuroscience267(2), 173–176.
  5. Tsukada, H., Harada, N., Nishiyama, S., Ohba, H., & Kakiuchi, T. (2000). Cholinergic Neuronal Modulation Alters Dopamine D2 Receptor Availability in vivo by Regulating Receptor Affinity Induced by Facilitated Synaptic Dopamine Turnover: Positron Emission Tomography Studies with Micro-dialysis in the Conscious Monkey Brain. Journal of Neuroscience20(18), 7067–7073.
  6. Vollenweider, F. X., Leenders, K. L., Øye, I., Hell, D., & Angst, J. (1997). Differential Psychopathology and Patterns of Cerebral Glucose Utilization Produced by (S)- and (R)-ketamine in Healthy Volunteers using Positron Emission Tomography (PET). European Neuropsychopharmacology7(1), 25–38.
  7. Prus, A. J., James, J. R., & Rosecrans, J. A. (2009). Conditioned Place Preference. In J. J. Buccafusco (Ed.), Methods of Behavior Analysis in Neuroscience (2nd ed.). CRC Press/Taylor & Francis.
  8. Yang, C., Shirayama, Y., Zhang, J. -c, Ren, Q., Yao, W., Ma, M., Dong, C., & Hashimoto, K. (2015). R-Ketamine: A Rapid-onset and Sustained Antidepressant Without Psychotomimetic Side Effects. Translational Psychiatry5(9), e632–e632.
  9. Hashimoto, K. (2020). Molecular Mechanisms of the Rapid-acting and Long-lasting Antidepressant Actions of (R)-ketamine. Biochemical Pharmacology177, 113935.
  10. Nahar, L., Delacroix, B. M., & Nam, H. W. (2021). The Role of Parvalbumin Interneurons in Neurotransmitter Balance and Neurological Disease. Frontiers in Psychiatry12.
  11. Yang, C., Han, M., Zhang, J., Ren, Q., & Hashimoto, K. (2016). Loss of Parvalbumin-Immunoreactivity in Mouse Brain Regions After Repeated Intermittent Administration of Esketamine, but not R-ketamine. Psychiatry Research239, 281–283.
  12. Yang, C., Kobayashi, S., Nakao, K., Dong, C., Han, M., Qu, Y., Ren, Q., Zhang, J., Ma, M., Toki, H., Yamaguchi, J., Chaki, S., Shirayama, Y., Nakazawa, K., Manabe, T., & Hashimoto, K. (2018). AMPA Receptor Activation–Independent Antidepressant Actions of Ketamine Metabolite (S)-norketamine. Biological Psychiatry84(8), 591–600. 
  13. Zimmermann, K. S., Richardson, R., & Baker, K. D. (2020). Esketamine as a Treatment for Pediatric Depression: Questions of Safety and Efficacy. The Lancet Psychiatry7(10), 827–829.
  14. Turner, E. H. (2019). Esketamine for Treatment-resistant Depression: Seven Concerns about Efficacy and FDA Approval. The Lancet Psychiatry6(12), 977–979.
  15. Leal, G. C., Bandeira, I. D., Correia-Melo, F. S., Telles, M., Mello, R. P., Vieira, F., Lima, C. S., Jesus-Nunes, A. P., Guerreiro-Costa, L. N. F., Marback, R. F., Caliman-Fontes, A. T., Marques, B. L. S., Bezerra, M. L. O., Dias-Neto, A. L., Silva, S. S., Sampaio, A. S., Sanacora, G., Turecki, G., Loo, C., … Quarantini, L. C. (2021). Intravenous Arketamine for Treatment-resistant Depression: Open-label Pilot Study. European Archives of Psychiatry and Clinical Neuroscience271(3), 577–582.

Silent Hypoxia in COVID-19 

Silent hypoxia is characterized by a significantly reduced oxygen saturation level with no associated breathing difficulties, at least in its beginning stages [1]. Because patients do not present with trouble breathing until the condition has progressed significantly, it can be difficult to detect [1]. Studies have recently reported that 20 to 40% of COVID-19 patients may experience silent hypoxia [1]. By the time medical teams have detected silent hypoxia, the patient may already have progressed into moderate-to-severe levels of infection, worsening their long-term recovery rates [2]. Consequently, medical practitioners must familiarize themselves with the warning signs of silent hypoxia to detect and treat it early. 

There are many possible reasons why COVID-19 patients may develop silent hypoxia and, subsequently, experience a deterioration of their ability to breathe. Researchers have posited various hypotheses, from the virus’s impact on blood vessels contributing to impaired hypoxic vasoconstriction to  changes to one’s respiratory system, perhaps via the expression of angiotensin-converting enzyme-2 receptors in the carotid bodies and nasal mucosa [1][3]. Unfortunately, while there are many possible theories concerning the development of this condition, research has not yet isolated the principal answer, making treatment more difficult [1].  

While the underlying mechanisms guiding the development of silent hypoxia may remain uncertain, researchers have made progress in identifying certain predictors for the condition. In a retrospective cohort study, Alhusain and colleagues analyzed data from all of the COVID-19 patients who visited a hospital in Riyadh, Saudi Arabia over ten months [4]. Among the 195 patients who experienced silent hypoxia, the researchers identified no correlations between dyspnea and gender, age group, comorbidity, or body mass index [4]. This finding was partially consistent with another study by Okhuama et al., who found that age and diabetes were non-predictors of silent hypoxia in COVID-19 patients and suggested that more complex mechanisms were at play [5]. However, Alhusain et al. did find that fever, cough, and chronic cardiac disease were predictors of dyspnea, providing medical teams with some guidance in anticipating the condition [4]. 

Medical teams can increase their chances of successfully identifying silent hypoxia by monitoring certain elements of the patient’s profile. Given that silent hypoxia patients may suffer from levels of pneumonia that are disproportionate to their COVID symptoms, practitioners should closely monitor patients’ pulse oximetry and arterial blood gas levels [5]. Bluish coloration can also indicate that a COVID-19 patient has silent hypoxia [6]. Before getting to the hospital setting, patients can also engage in detection practices themselves by regularly checking their blood saturation levels using a pulse oximeter or a smartphone [2]. A drop in oxygen saturation levels below 95% warrants contacting a health provider [2]. 

Ultimately, silent hypoxia is a pressing condition that can increase rates of intubation, mechanical ventilation, and even death among COVID-19 patients [2]. While medical teams still await more information about silent hypoxia, heeding the aforementioned indications can help treat pandemic patients and, moreover, suppress the adverse impacts of this ongoing pandemic. 


[1] A. Rahman et al., “Silent hypoxia in COVID-19: pathomechanism and possible management strategy,” Molecular Biology Reports, vol. 48, no. 4, p. 3863-3869, April 2021. [Online]. Available:

[2] J. Teo, “Early Detection of Silent Hypoxia in Covid-19 Pneumonia Using Smartphone Pulse Oximetry,” Journal of Medical Systems, vol. 44, no. 8, p. 1-2, June 2020. [Online]. Available:

[3] T. Fuehner et al., “Silent Hypoxia in COVID-19: A Case Series,” Respiration, vol. 101, p. 376-380, November 2021. [Online]. Available:

[4] F. Alhusain et al., “Predictors and clinical outcomes of silent hypoxia in COVID-19 patients, a single-center retrospective cohort study,” Journal of Infection and Public Health, vol. 14, no. 11, p. 1595-1599, November 2021. [Online]. Available:

[5] A. Okuhama et al., “Clinical and radiological findings of silent hypoxia among COVID-19 patients,” Journal of Infection and Chemotherapy, vol. 27, no. 10, p. 1536-1538, October 2021. [Online]. Available:

[6] T. S. Simonson et al., “Silent hypoxaemia in COVID-19 patients,” The Journal of Physiology, vol. 599, no. 4, p. 1057-1065, December 2020. [Online]. Available:


Anesthesia Considerations for Balloon Sinuplasty

In 2005, the FDA approved balloon sinus ostial dilation–also known as balloon sinuplasty, or BSD–for use in treating both recurrent acute and chronic rhinosinusitis [1]. This technique involves placing a balloon catheter into the sinus ostium; the resultant inflation dilates the sinus opening and subsequently relieves obstructions [1]. Since becoming FDA-approved, several studies have confirmed the safety of balloon sinuplasty procedures and have discovered additional benefits, including, but not limited to, avoidance of general anesthesia in certain cases [1]. 

During balloon sinuplasty, a patient requires anesthesia [2]. When the procedure was first introduced, patients typically received general anesthesia by way of an endotracheal tube or a laryngeal mask airway [2]. However, since its introduction, sedation and local anesthesia have become more common, facilitating a transition to office-based procedures [2]. Compared with sinus surgery performed under general anesthesia, local anesthesia-based balloon sinuplasty has the advantages of greater convenience, quicker recovery, similar technical success, and lower costs [3]. 

In a recent study, Naik et al. compared local and general anesthesia [4]. They split their 50 subjects into two evenly sized groups: one that underwent BSP with general anesthesia, while the other received a combined nerve block and topical anesthesia regimen [4]. The researchers found that the local anesthesia group experienced a shorter time gap between when the patient entered the operating theater and when the surgical procedure began; they also recovered quicker [4]. However, this group reported feeling more intraoperative discomfort than the general anesthesia group [4]. Additionally, surgeons performing local anesthesia were less comfortable than those treating the general anesthesia patients [4]. Nevertheless, Naik and colleagues concluded that, for “less apprehensive and motivated cases,” anesthesia providers can opt for local anesthetics which, along with promoting quicker results, are also the more cost-effective option [4].

Although it is considered an alternative to endoscopic sinus surgery (ESS), BSD is more accurately described as another tool, device, or instrument available to physicians performing ESS [1]. Instead of placing a balloon in the sinuses, physicians performing traditional ESS place an endoscope or, in more difficult cases, more specialized instruments to clear drainage pathways and potentially straighten the septum. [5]. Despite being less invasive than ESS, BSD has significant similarities with ESS in terms of anesthetic techniques [6, 7]. Therefore, when considering best anesthetic practices to use in conjunction with BSD, guidelines regarding anesthesia administration during ESS may also be relevant for anesthesia providers performing general anesthesia-based BSD.

Accordingly, anesthesia providers should take steps to avoid or minimize surgical bleeding [8]. To minimize the occurrence of surgical bleeding–the most serious form of which is capillary bleeding–some research points toward avoiding volatile anesthetic agents, which cause vasodilation, where possible [8]. Additionally, maintaining anesthesia depth by providing patients with muscle relaxants and limiting the use of positive end-expiratory pressure can prevent higher intrathoracic pressure, which increases surgical bleeding from the head [8]. Maintaining normothermia is also important for minimizing bleeding, as is administering local anesthetics and vasoconstrictors [8].

Researchers are optimistic that, in the future, patients may require minimal to no anesthesia when undergoing balloon sinuplasty [2]. While anesthetics are still necessary, opting against general anesthesia when possible and, when it is not, minimizing surgical bleeding is important to the success of BSD-based surgeries.


[1]  C. Cingi, N. Bayar Muluk, and J. T. Lee, “Current indications for balloon sinuplasty,” Current Opinion in Otolaryngology & Head and Neck Surgery, vol. 27, no. 1, p. 7-13, February 2019. [Online]. Available:

[2]  A. E. Stewart and W. C. Vaughan, “Balloon Sinuplasty Versus Surgical Management of Chronic Rhinosinusitis,” Current Allergy and Asthma Report, vol. 10, 1, p. 181-187, March 2010. [Online]. Available:

[3]  J. Gould et al., “In-Office, Multisinus Balloon Dilation: 1-Year Outcomes from a Prospective, Multicenter, Open Label Trial,” American Journal of Rhinology & Allergy, vol. 28, no. 2, p. 156-163, March-April 2014. [Online]. Available:

[4]  S. S. Naik, C. Venkategowda, N. Reddy, and S. M. Naik, “Combined Nerve Block and Topical Anesthesia: An Effective Alternate to General Anesthesia in Hybrid Balloon Sinuplasty Procedures,” Journal of Research & Innovation in Anesthesia, vol. 5, no. 1, p. 6-9, January-June 2020. [Online]. Available:

[5] “Balloon Sinuplasty v. Endoscopic Sinus Surgery Explained,” Kaplan Sinus Relief, Updated October 23, 2020. [Online]. Available:

[6]  A. Koskinen et al., “Comparison of intra-operative characteristics and early post-operative outcomes between endoscopic sinus surgery and balloon sinuplasty,” Acta Oto-Laryngologica, vol. 137, no. 2, p. 202-206, April 2018. [Online]. Available:

[7]  J. Flávio Nogueira Júnior, A. C. Stamm, and S. Pignatari, “Balloon sinuplasty, an initial assessment: 10 cases, results and follow-up,” Brazilian Journal of Otorhinolaryngology, vol. 76, no. 5, p. 588-595, September/October 2010. [Online]. Available:

[8]  P. Y. Tan and R. Poopalalingam, “Anaesthetic Concerns for Functional Endoscopic Sinus Surgery,” Proceedings of Singapore Healthcare, vol. 23, no. 3, p. 246-253, 2014. [Online]. Available:


Anesthesiology vs. Pain Medicine

Historically, pain medicine was a subset of the general field of anesthesiology [1]. With the advent of nerve procedures, however, the two disciplines evolved to encompass increasingly separate, but nevertheless interrelated, functions [1]. These two fields have differing roles, educational requirements, and treatment options.

Pain medicine doctors, also referred to as pain management doctors, specialize in the diagnosis, management, and treatment of pain and painful disorders [2]. They assist patients with varying pain levels, ranging from acute to chronic [2]. Alternatively, anesthesiologists are experts in providing medical care for patients at every step of surgery [3]. Their major focus is sustaining life function during operations, which means that they are trained in pain management, but approach pain from a specific perspective [3].

There are two categorizations within the overall discipline of pain medicine: “medical pain” and interventional [1]. Medical pain is the broader category. Practitioners in this field can include family medicine doctors, internists, and psychiatrists [1]. Accordingly, they come from a diverse range of educational backgrounds–pain medicine doctors may have completed residencies in neurology, psychiatry, rehabilitation, or physical medicine, among other disciplines [2]. They primarily work with people who suffer from chronic ailments and, therefore, may require long-term medical treatment and, in some cases, opioids or other medications [1]. These doctors can prescribe a varied range of treatment options, either separately or in combination, to alleviate patients’ pain [4]. For instance, physicians may recommend interdisciplinary treatment plans that combine physical therapy, psychotherapy, and acupuncture [4].

While the distinction between anesthesiologists and the doctors providing care for pain relief as described above is evident, the boundary between pain medicine and anesthesiology is more blurred when considering interventional pain physicians. Interventional doctors treat their patients by way of more complicated pain management procedures and techniques [1]. They can administer spine injections, nerve blocks, and implantable devices [1]. As such, they are often trained in anesthesiology. In the United States, interventional pain management physicians must finish one year of internship, a residency in either anesthesiology, neurology, psychiatry or rehabilitative medicine, and a one-year-long fellowship in pain management [1].

Today, there remains some debate about the intersection between anesthesiology and pain management, most notably pertaining to the treatment of chronic pain. Anesthesiologists receive specialized training in acute pain, but they do not necessarily study chronic pain management [5]. As a result, some physicians have advocated for educational reform that would either incorporate chronic pain training into the anesthesiology curriculum or further distinguish chronic pain treatment from anesthesiology [5]. While it is unclear which path the medical community will take, the dual training that many interventional pain doctors receive in anesthesiology and pain management appears to be a step in the right direction.

Millions of patients experience pain every year [6]. Fortunately, anesthesiologists and pain management doctors can offer a diverse range of treatment options to their patients. By keeping in mind the respective strengths of these two classes of practitioners, patients will hopefully have a greater chance of receiving appropriate and effective pain relief.


[1] “What Does a Pain Management Doctor Do?,” Integris Health, Updated September 21, 2020. [Online]. Available:

[2] S. Lewis, “Pain Medicine Doctor: Your Pain Relief & Pain Management Specialist,” Healthgrades, Updated December 21, 2017. [Online]. Available:

[3] S. Lewis, “Anesthesiologist: Your Surgical Anesthesia & Pain Management Specialist,” Healthgrades, Updated January 21, 2020. [Online]. Available:

[4] “What does a pain management doctor do?,”, Updated August 24, 2021. [Online]. Available:

[5] J. D. Loeser, “The Education of Pain Physicians,” Pain Medicine, vol. 16, no. 2, p. 225-229, February 2015. [Online]. Available:

[6] R. Sinatra, “Causes and Consequences of Inadequate Management of Acute Pain,” Pain Medicine, vol. 11, no. 12, p. 1859-1871, December 2010. [Online]. Available:


Anesthesia Considerations for Thyroid Surgery 

The thyroid is a gland located in the anterior region of the neck and is a critical part of the endocrine system.1 Specifically, the thyroid secretes the hormones T3 and T4, which increase the body’s basal metabolic rate, and calcitonin, which lowers blood calcium.2 Partial or complete removal of the thyroid in an operation known as a thyroidectomy may be recommended when cancer is detected or suspected to exist in the thyroid.3 Thyroid surgery may range from the simple removal of a small nodule from the thyroid to a more complicated operation to relieve the trachea from the pressure caused by a goiter (swelling of the neck resulting from enlargement of the thyroid), and the optimal anesthesia approach is affected by the type of surgery as well as patient factors.

Several different anesthesia options exist for thyroid surgery. Regional anesthesia has been shown to be effective and safe, though it is more often used for procedures on smaller scales.4 More common for a thyroidectomy, however, is general anesthesia. When tracheal compression is occurring, anesthesia can usually be administered without any impediments, however, a patient may be induced into the semi-supine or sitting position or, in more extreme cases, undergo fiberoptic intubation if needed.5 Pre-oxygenation with 100% oxygen should precede muscle relaxation for general anesthesia.

Total intravenous anesthesia, which is the use of intravenous agents only for the induction and maintenance of anesthesia, is commonly used during thyroid surgery.6 Propofol is among the most effective anesthetic agents, as it provides a rapid onset of anesthesia, does not have an extended recovery time, and has a low incidence of postoperative nausea.7 Opioids are often co-administered to potentiate their effect: the combination of propofol with the opioid remifentanil provides a short duration of action that can be easily targeted as well as adjusted for specific patient needs.8

There are several potential postoperative complications that anesthesiologists must be careful to detect and prevent from developing. One such complication is recurrent laryngeal nerve (RLN) palsy, a condition in which the recurrent laryngeal nerves that control the muscles of the larynx become injured, which can result in hoarseness, difficulty breathing, and physical exhaustion.9 While permanent nerve palsy occurs in less than 2% of patients undergoing thyroid surgery, temporary palsy has been reported in 3-10% of patients.10 The condition can be brought about by contusion to or clamping of the nerves during intubation and extubation, and, as such, anesthesiologists traditionally inspect the vocal cords immediately after extubation.5 Since this is often technically difficult, anesthesiologists can use a fiberscope or electrophysiological monitoring to prevent damage to the RLNs.11 An additional potential postoperative complication is postoperative hemorrhage, which can be avoided by maintaining hemostasis. Anesthesiologists typically maintain the patient’s intrathoracic pressure for 10-20 seconds to ensure that hemostasis has been achieved before the wound is closed.7

The parathyroid is a gland adjacent to the thyroid that maintains calcium homeostasis, and a parathyroidectomy, like a thyroidectomy, is a common surgical procedure for parathyroid swelling. In contrast to the thyroidectomy, however, local anesthesia is typically used for a parathyroidectomy, which may involve cervical nerve blocks.5 Nerve blocks may be deep or superficial, though no significant differences in postoperative pain and patient satisfaction have been found between the two types.


1. Beynon, M. E. & Pinneri, K. An Overview of the Thyroid Gland and Thyroid-Related Deaths for the Forensic Pathologist. Acad. Forensic Pathol. 6, 217–236 (2016). 

2. How does the thyroid gland work? [Internet] (Institute for Quality and Efficiency in Health Care (IQWiG), 2018). 

3. Thyroid Surgery. American Thyroid Association

4. Hisham, A. N. & Aina, E. N. A reappraisal of thyroid surgery under local anaesthesia: back to the future? ANZ J. Surg. 72, 287–289 (2002). 

5. Malhotra, S. & Sodhi, V. Anaesthesia for thyroid and parathyroid surgery. Contin. Educ. Anaesth. Crit. Care Pain 7, 55–58 (2007). 

6. Total Intravenous Anaesthesia – an overview | ScienceDirect Topics.

7. Bacuzzi, A. et al. Anaesthesia for thyroid surgery: Perioperative management. Int. J. Surg. 6, S82–S85 (2008). 

8. Lentschener, C. et al. Remifentanil-propofol vs. sufentanil-propofol: optimal combinations in clinical anesthesia. Acta Anaesthesiol. Scand. 47, 84–89 (2003). 

9. Paquette, C. M., Manos, D. C. & Psooy, B. J. Unilateral Vocal Cord Paralysis: A Review of CT Findings, Mediastinal Causes, and the Course of the Recurrent Laryngeal Nerves. RadioGraphics 32, 721–740 (2012). 

10. Rafiq, M., Al-Zoraigi, U., Alzahrani, S. & Alabdulkarim, Y. A Case of Transient Local Anesthetic Induced Bilateral Vocal Cord Palsy. Case Rep. Surg. 2015, 379258 (2015). 

11. Tanigawa, K., Inoue, Y. & Iwata, S. Protection of recurrent laryngeal nerve during neck surgery: a new combination of neutracer, laryngeal mask airway, and fiberoptic bronchoscope. Anesthesiology 74, 966–967 (1991). 


Antibodies After COVID-19 Infection

The COVID-19 pandemic, caused by the virus SARS-CoV-2, is still a global problem. Research on protection due to antibodies after COVID-19 infection (and vaccination) can contribute to clinical knowledge and more informed public health strategies.

Antibodies, also called immunoglobulins (Ig), are created by the plasma cells (mature B cells) of the immune system. The antibodies recognize and bind to a specific pattern or structure, called the antigen. Antibodies prevent harm by neutralizing a pathogen’s ability to enter cells or by marking the pathogen for attack by specialized immune cells (Durani, 2014). After a first infection, the body will keep some of the plasma cells as memory B cells, so that if the pathogen is encountered again, the antibody response will be quicker and more powerful (Cagiga et al, 2021).

The body makes five different types of antibodies: IgG, IgM, IgA, IgE and IgD. IgG is the most common antibody type and is a smaller protein that is found throughout the body. IgM is the first antibody type made upon infection and is found primarily in blood and lymph fluid. IgA is found mostly in mucous membranes, including in the respiratory tracts. IgE is mostly seen in allergic reactions, and IgD exists in only small amounts and its purpose is not understood (Durani, 2014). IgG, IgM and IgA are the types of antibodies that are relevant to SARS-CoV-2 infection.

For SARS-CoV-2, the antibody can attach to an antigen from either the virus’s spike glycoprotein (S antibodies) or nucleocapsid protein (N antibodies). The virus’s spike protein contains the receptor binding domain (RBD) that the virus uses to enter host cells; S antibodies against the RBD are more likely to be neutralizing (Cagiga et al, 2021). A neutralizing antibody prevents the virus from entering the host cell and reproducing. In comparison to S antibodies, N antibodies have not been found to provide protection against infection (Cagiga et al, 2021).

In response to COVID-19 infection, IgM antibodies are produced first throughout the body; it reacts strongly to antigens (high avidity) and ultimately represents 10% of the serum antibodies. IgG appears later and has high capacity for neutralization (Zhu et al, 2021). IgG and IgA are also produced locally from cells in the airway. IgA from the airway has been seen to peak at high levels early in infection and then begin to decline. Airway IgG and IgA levels waned significantly by 3 months post-infection in a study of 147 patients (Cagiga et al, 2021). Systemic IgM levels also declined significantly by the third month, and systemic IgG levels were observed to slightly decline (Zhu et al, 2021).

Despite declining levels, a high percentage of patients were still seropositive for IgG seven months after infection; in other words, they still had significant IgG reaction against a SARS-CoV-2 challenge. IgG antibodies after COVID-19 infection may stay in the body for up to two years (Zhu et al, 2021). It was also found that around 25% of patients still were seropositive for IgM after 6 to 9 months. However, all antibodies were found to decrease in neutralizing ability over time (Zhu et al, 2021).

In addition to antibody type, levels, and neutralizing ability, antibody avidity also plays a role in effectiveness. Avidity is how strongly the antibody binds to its antigen. With SARS-CoV-2, antibody avidity increased three months after infection when antibody levels started to decline, in a process called avidity maturation. High avidity antibodies may be associated with a lower risk of reinfection (Löfström et al, 2021).

Antibodies after recovery from COVID-19 were seen to vary based on disease severity. Patients recovering from a severe or critical disease were seropositive for IgG and IgM after approximately 7 months at a significantly higher rate than patients with asymptomatic infection (Zhu et al, 2021). Patients with low viral loads in the respiratory tract also may not develop antibodies at all (non-seroconversion) (Liu et al, 2021).

Age also impacted antibodies after recovery. Kids and adolescents were found to have the lowest rates of seropositivity for IgG and IgM, with adults under 60 having the highest rates and adults older than 60 falling in between. Luckily, children were more likely to have a less violent immune response and only mild symptoms, if any at all (Liu et al, 2021).


Cagigi A, Yu M, Österberg B, et al. Airway antibodies emerge according to COVID-19 severity and wane rapidly but reappear after SARS-CoV-2 vaccination. JCI Insight. 2021;6(22):e151463. Published 2021 Nov 22. doi:10.1172/jci.insight.151463 

Löfström E, Eringfält A, Kötz A, et al. Dynamics of IgG-avidity and antibody levels after Covid-19. J Clin Virol. 2021;144:104986. doi:10.1016/j.jcv.2021.104986 

Liu W, Russell RM, Bibollet-Ruche F, et al. Predictors of Nonseroconversion after SARS-CoV-2 Infection. Emerg Infect Dis. 2021;27(9):2454-2458. doi:10.3201/eid2709.211042. 

Durani Y. Blood Test: Immunoglobulins (IgA, IgG, IgM). Rady Children’s Hospital San Diego- 2014.

Zhu L, Xu X, Zhu B, et al. Kinetics of SARS-CoV-2 Specific and Neutralizing Antibodies over Seven Months after Symptom Onset in COVID-19 Patients. Microbiol Spectr. 2021;9(2):e0059021. doi:10.1128/Spectrum.00590-21


Controversy Over “No Surprises Act” Implementation

Last December, Congress passed the “No Surprises Act” to shield patients from unexpected bills incurred when they receive medical treatment from providers outside their insurance networks. The bipartisan bill was applauded by groups like the American Hospitals Association,1 as well as consumers frustrated with the long history of “balance billing” in the United States — a process in which out-of-network providers bill individuals for the charges not covered by their insurance plans. The “No Surprises Act” attempts to remove patients from the center of these conflicts by establishing an independent dispute resolution process between insurers and providers.2 But as Congress finalizes the details of the implementation of the No Surprises Act, many providers are protesting new guidelines they argue will benefit insurers at the expense of patients and providers.3 

Patients often encounter surprise bills in emergency settings, when they go to (or are taken to) a facility without consideration of their insurance plan due to a focus on quickly receiving definite care. A 2017 study found that patients who received surprise bills for emergency care paid ten times as much as those who did not, and that roughly 18 percent of emergency visits resulted in at least one out-of-network bill.4 But surprise bills can also appear when patients go to an in-network facility but receive care from an out-of-network provider, such as an anesthesiologist, surgical assistant, or ambulatory service.2 Roughly one in five privately insured patients undergoing an elective surgery at in-network hospitals received such a bill, according to a 2020 study. This was often attributed to anesthesiology expenses, with an average out-of-network bill of $1,219 in the study.4  

According to a new rule of the No Surprises Act, a particular benchmark — the qualifying payment amount (QPA) — should serve as a “starting point” in making payment determinations, as this number is “generally the plan or issuer’s median contracted rate for the same or similar service in the specific geographic area,” according to the Centers for Medicare and Medicaid Services (CMS).2 Parties can submit additional information if they wish to make an offer that deviates from the QPA-based offer, but it “must clearly demonstrate that the value of the item or service is materially different from the QPA,” according to the CMS.2  

Now, members of Congress are arguing that prioritizing the QPA over other considerations (physician’s training, quality of outcomes, local market share of the parties involved, etc.), will give insurers in upper hand in the dispute resolution process. Relying on the QPA may incentivize insurers to set artificially low payment rates, putting pressure on small practices, like anesthesiology practices, and limiting patients’ access to care. Over 150 lawmakers — nearly half of them Democrats, and some of them doctors themselves — signed a letter citing their opposition to the new rule.3 

Also speaking out against the rule are leading physician societies, including the American Society of Anesthesiologists (ASA). These societies argue that the QPA is calculated by the insurance companies “without meaningful oversight or transparency,” and therefore can be manipulated in their favor without reflecting actual payment rates, thereby undermining the spirit of the legislation, which emphasizes information sharing and the equal consideration of multiple factors.For this reason, some health care experts have emphasized that “rule makers should prioritize, strengthen, and highlight full historical context for arbiters and emphasize this information-sharing provision in final rulemaking for the arbitration process.”6 

Already, the ASA is protesting actions believed to be driven by insurers’ desires to maintain the upper hand in forthcoming disputes. According to the ASA, Blue Cross Blue Shield of North Carolina threatened in a letter to anesthesiology and physician practices that their contract and in-network status would be terminated unless they immediately agreed to payment reductions ranging from 10% to over 30%, with the No Surprises Act cited as driving the reduction. To many, this shows how the new rule may allow insurance companies to leverage their market power to prioritize their finances, pushing providers out of insurance networks or forcing them to accept lower rates along the way.7 It may particularly harm networks in rural and underserved areas by incentivizing insurers to push down the rates they pay to in-network providers.3 

Still, in some areas, a united group of providers may be stronger than the insurers in the market, allowing them to take the upper hand. The Congressional Budget Office also reports that patients may enjoy lower premiums, reduced by an estimated 1%, as a result of the act.3 If the act is passed with these provisions, it ultimately remains to be seen what effect it will have. 


  1. Detailed summary of No Surprises Act. (2021, January 14). American Hospitals Association. 
  1. Requirements Related to Surprise Billing; Part II interim final rule with comment period. (2021, September 30). Centers for Medicare and Medicaid Services. 
  1. McAuliff, M. (2021, November 17). Congressional doctors lead bipartisan revolt over policy on surprise medical bills. Kaiser Health News. 
  1. Office of the Assistant Secretary for Planning and Evaluation. (2021, November 22). Evidence on Surprise Billing: Protecting Consumers with the No Surprises Act. U.S. Department of Health and Human Services. 
  1. Nation’s frontline physicians denounce regulators’ implementation of key rule in No Surprises Act. (2021, October 1). American Society of Anesthesiologists.–key-rule-in-no-surprises-act 
  1. Koski-Vacirca, R., & Venkatesh, A. (2021, November 2). Rulemaking for health care affordability: Implementing the No Surprises Act. Health Affairs.  
  1. Lagasse, J. (2021, November 23). American Society of Anesthesiologists accuses BCBSNC of abusing No Surprises Act. Healthcare Finance News.